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MicroRNA-29a-3p Downregulation Causes Gab1 Upregulation to Promote Glioma Cell Proliferation

Cellular Physiology and Biochemistry. 2018;48(2):450-460 DOI 10.1159/000491776

 

Journal Homepage

Journal Title: Cellular Physiology and Biochemistry

ISSN: 1015-8987 (Print); 1421-9778 (Online)

Publisher: Cell Physiol Biochem Press GmbH & Co KG

LCC Subject Category: Science: Physiology | Science: Chemistry: Organic chemistry: Biochemistry

Country of publisher: Germany

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS


Nai-yuan Shao

Dong-xing Wang

Yin Wang

Ya Li

Zhi-qing Zhang

Qin Jiang

Weifeng Luo

Cong Cao

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 16 weeks

 

Abstract | Full Text

Background/Aims: Glioma causes significant human mortalities annually. Molecularly-targeted therapy is a focus of glioma research. Methods: Grb2-associated binding 1 (Gab1) expression and microRNA-29a-3p (“miR-29a-3p”) expression in human glioma cells and tissues were tested by Western blotting assay and qRT-PCR assay. shRNA/siRNA strategy was applied to silence Gab1 in human glioma cells. miR-29a or anti-sense miR-29a construct was transfected to human glioma cells. Cell proliferation was tested by BrdU ELISA assay and cell counting assay. Results: We show that expression of Gab1 was significantly elevated in human glioma tissues and cells, which correlated with downregulation of its putative microRNA: miR-29a-3p. In A172 glioma cells and primary human glioma cells, Gab1 shRNA/siRNA inhibited Akt-Erk activation and cell proliferation. Forced-expression of miR-29a-3p downregulated Gab1, inhibiting glioma cell proliferation, whereas miR-29a-3p was in-effective on cell proliferation in Gab1-silenced A172 cells. Furthermore, introduction of a 3’-untranslated region (3’-UTR) mutant Gab1 (UTR-G160A) blocked miR-29a-3p-induced inhibition on Akt signaling and A172 cell proliferation. Conclusions: miR-29a-3p downregulation leads to Gab1 upregulation to promote glioma cell proliferation.